This research proposal will investigate the hypothesis that nutritional deficiencies of selenium, copper, or vitamin E predispose rats to oxidant lung damage by decreasing normal cellular defenses. Selenium deficiency decreases the activity of the copper-dependent enzyme superoxide dismutase (SOD) as well as the activity of Se GSH-Px. Vitamin E deficiency results in decreased intracellular ability to scavenge free radical products of oxygen reduction. These three nutritional groups, plus matched controls, will be exposed in an oxygen chamber to either 21 percent inspired O2 (room air) or 85 percent inspired O2 (hyperoxia) at STP. Data will be obtained concerning mortality, lung pathology, lung weights, and lung supernatant enzyme activity of SOD, Se GSH-Px, catalase, and glutathione S-transferase (GSH S-transferase). Several of the GSH S-transferases have been shown to exhibit a non-selenium-dependent glutathione peroxidase activity which can block lipid peroxidation and make these enzymes potentially important in protecting against oxidant lung damage. These nutritional groups will be characterized according to baseline enzyme activities and changes in enzyme activity after a hyperoxic exposure. We will also attempt to determine if the mechanism of lung damage is due to lipid peroxidation. Ethane production, measured gas chromatographically in metabolic chambers after oxygen administraton, will serve as an index of lipid peroxidation. Tissue levels of lipid peroxides will be measured if ethane production is undetectable. Lung damage will be assessed histologically and comparison will be made between the extent of pathologic damage and the amount of lipid peroxidation measured.